MiR-185-5p is Involved in Regulating the Abnormal Proliferation of Retinal Microvascular Endothelial Cells via

Xiaoxia Wen1, Yunxia Tang2, Hongjian Guo2

  • 1Department of Ophthalmology, The People's Hospital of Kaizhou District, Chongqing, China.

Current Eye Research
|November 25, 2024
PubMed
Abstract

Insights

MicroRNA-185-5p is elevated in proliferative diabetic retinopathy (PDR) and may help diagnose PDR. It also influences retinal endothelial cell behavior by targeting CXCR4.

Area of Science:

  • Ophthalmology
  • Molecular Biology
  • Biochemistry

Background:

  • Diabetic retinopathy (DR) is a leading cause of vision loss.
  • Proliferative diabetic retinopathy (PDR) is an advanced stage characterized by neovascularization.
  • Understanding the molecular mechanisms underlying PDR is crucial for developing effective treatments.

Purpose of the Study:

  • To investigate the expression profile of miR-185-5p in PDR.
  • To evaluate the diagnostic potential of miR-185-5p for PDR.
  • To elucidate the role and mechanism of miR-185-5p in PDR pathogenesis.

Main Methods:

  • Quantitative reverse transcription polymerase chain reaction (qRT-PCR) for miR-185-5p expression.
  • Receiver operating characteristic (ROC) curve analysis for diagnostic evaluation.
  • Transwell and CCK-8 assays to assess cell migration and proliferation.
  • Enzyme-linked immunosorbent assay (ELISA) for inflammatory factors.
  • Luciferase reporter gene assay to confirm target interaction.

Main Results:

  • miR-185-5p was significantly upregulated in type 2 diabetes mellitus (T2DM) and PDR patients, with higher levels in PDR.
  • Serum miR-185-5p demonstrated diagnostic capability to distinguish PDR from T2DM.
  • High glucose increased miR-185-5p expression, promoting HREC migration, proliferation, and inflammation.
  • Inhibition of miR-185-5p reversed these effects.
  • miR-185-5p directly targets CXCR4.

Conclusions:

  • miR-185-5p expression is dysregulated in PDR.
  • miR-185-5p may play a role in PDR development by regulating HREC migration and proliferation via CXCR4.